Urinary tract infections (UTIs) are a frequent health issue, particularly for women. Nearly half of all women experience a UTI at some point in their lives.
These infections are uncomfortable and often painful, largely due to a type of bacteria known as Escherichia coli, or E. coli.
Scientists have long been puzzled by how these bacteria manage to thrive and reproduce rapidly inside the human bladder, considering that fresh urine is almost completely free of nutrients.
At the University of Michigan Medical School, a team led by Harry Mobley, a respected microbiology and immunology professor, has been investigating this phenomenon.
Their research focuses on the strategies E. coli uses to survive and grow inside the bladder, where nutrients are scarce. One of their main discoveries is that E. coli can either produce its own nutrients or steal them from the host by using special systems called transport systems.
These transport systems are quite efficient. Mobley’s team found that about a quarter of the genes in the E. coli bacteria are devoted to these systems, which help pull in vital nutrients like amino acids at an astonishing rate.
By studying mutant strains of E. coli that were less effective at replicating in laboratory mice, the researchers identified several genes responsible for these nutrient transport systems as key players in the bacteria’s ability to cause infections.
Allyson Shea, a former member of Mobley’s team and now an assistant professor herself, took this research a step further. She compared the E. coli transport proteins with those from other UTI-causing bacteria.
Shea discovered that a specific type called ABC transporters, which stands for ATP-binding cassette transporters, were crucial for infection. These transporters use energy from a molecule called ATP to pull nutrients through the bacterial cell wall.
Using a special gel made from mouse urinary tract cells, Shea demonstrated that bacteria lacking these ABC transporters couldn’t grow well on this nutrient-poor medium.
This indicated that these transporters are not just beneficial but essential for the bacteria’s survival and growth.
The implications of these findings are significant, especially at a time when many bacteria are becoming resistant to traditional antibiotics. Mobley suggests that targeting these ABC transporters might be a way to control bacterial growth.
Slowing down their ability to import nutrients could make it easier for antibiotics and the human immune system to fight the infection.
However, it’s not a straightforward task. According to Shea, bacteria have developed multiple backup systems for these transporters, making it challenging to completely shut them down.
But there is potential in targeting a common component of these transporters, the ATP-binding subunit, which could disrupt their function across the board.
This approach wouldn’t necessarily eliminate the need for antibiotics but could enhance their effectiveness by slowing the bacteria’s growth, giving both drugs and the immune system a better chance to work.
This research marks a promising step toward developing new treatments for UTIs, offering hope for better management of this common ailment in the future.
Alongside Mobley and Shea, other contributors to this study include Valerie S. Forsyth, Jolie A. Stocki, Taylor J. Mitchell, Arwen E. Frick-Cheng, Sara N. Smith, and Sicily L. Hardy, all of whom have added valuable insights into the complex interactions between bacteria and their hosts.
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The research findings can be found in PNAS.
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